TONIC CHEMOREFLEX ACTIVATION DOES NOT CONTRIBUTE TO ELEVATED MUSCLE SYMPATHETIC-NERVE ACTIVITY IN HEART-FAILURE

Background Sympathetic activation in heart failure may be due to an in crease in sympathetic excitatory influences or to a decrease in inhibi tory signals to the brain stem. Chemoreflex sensitivity may be increas ed in patients with heart failure. The present study tested the hypoth esis that tonic activation of excitatory chemoreceptor afferents contr ibutes to the elevated sympathetic activity in heart failure. Methods and Results We recorded sympathetic nerve activity to muscle circulati on from the peroneal nerve of 12 chronic heart failure patients while the patients were breathing room air and during deactivation of the ch emoreceptors while the patients were breathing a 100% O-2 gas mixture. All patients except 2 were in class III of the New York, Heart Associ ation functional classification. Left ventricular ejection fraction de fined by radionuclide ventriculography was 24+/-2% (mean+/-SE). We als o obtained measurements of resting sympathetic nerve activity in 9 hea lthy control subjects to document that sympathetic nerve activity was elevated in heart failure subjects. Resting sympathetic nerve activity was 59+/-5 bursts/min in heart failure patients versus 36+/-4 bursts/ min in control subjects (P<.01). In heart failure patients, oxygen adm inistration increased oxygen saturation from 94+/-0.9% to 99+/-0.3% (P <.0001). This increase in oxygen saturation did not affect resting mus cle sympathetic nerve activity (798+/-122 U/min while patients breathe d room air and 824+/-35 U/min during 100% O-2 breathing) or blood pres sure. Conclusions Increased efferent sympathetic activity to muscle ci rculation in patients with heart failure is not explained by tonic act ivation of excitatory chemoreflex afferents.